Little is known about the reflex effect on airway caliber of static muscular contraction. In addition, little is known about the discharge properties of the group III (ADelta) and IV (C) muscle afferents that are both stimulated by static contraction and are believed responsible for the reflex autonomic effects caused by this stimulus. Therefore, the proposed research will attempt to determine if static contraction of the hindlimb reflexly dilates the airways. If static contraction does cause reflex dilation of the airways, then it will be determined whether this dilation is due to cholinergic withdrawal or to Beta-adrenergic excitation. Also, the proposed research will attempt to characterize the metabolic and/or mechanical stimuli that discharge the group III and IV muscle afferents whose stimulation reflexly evokes the contraction-induced airway dilation. In all experiments, static contraction will be induced by electrically stimulating the cut peripheral ends of the L7-S1 ventral roots of chloralose-anesthetized cats. Changes in airway caliber will be measured by recording both changes in trachealis muscle tension and changes in total pulmonary resistance. Changes in afferent input will be measured by recording changes in single fiber impulse activity from the L7-S1 dorsal roots. The proposed research may provide new information about the reflex airway response to static exercise as well as the afferents causing that response.